LT46-47
33 important questions on LT46-47
What is key enzym in fibrinolysis?
Normally you have covalent cross-linked fibrin generated by means of coagulation factor keratin.
Plasmin degrades this structure between D and E domains, and this results in the formation of D-dimers. If you measure the D-dimers, you know fibronlysis is going on.
What is venous thrombosis and fibrinolysis?
Therapy is targeting coagulation (heparin/vitamin K antagonists)
Primary aim: preventing occurence of a pulmoary embolism.
Resolution of the thrombus: warranted by endogenous fibrionlyssi
What is arterial thrombosis and fibrionlysis?
may obstruct arterial flow
Impact depdnent on rate of thrombus removal by fibrinolysis.
You can do this endogenous fibrinolysis or phamracoligcally fibrinolysis.
Atherosclerotic plaque indcues activation of hemostasis.
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What are the main particles involved in atheroscleriss?
How can trapping of excess LDL be enhanced?
High glucose
High blood pressure
Chemotherapy
Infections
Radiations
How do you get endothelial dysfunction?
Prolonged half-life of LDL results in LDL oxidation
OxLDL is toxic and affects cells of the arterial wall
It induces
- activation o endothelium and expression of cell adhesion molecules, signaling molecules that there is a toxic portein
- adhesion, transmigration and retention of cells involved in inflammation (monocytes), aim to remove the toxic LDL expressing
What is step II of atherosclerosis?
OxLDL loaded macrophages are unable to leave the vessel wall
If there is a continuous influx of high levels of LDL, these macropahges become sort of obese, that they cannot return back to the circulation and deliver it to the liver. They get stuck in the vessel wall. You get macrophage foam cell formation.
The first visible stage is a fatty streak.
What is step III of atherosclerosis?
As a healing response SMC prolliferate and migrate.
SMC produce collagen and elastin
Formation of a protective SMC rich fibrous cap
What is step IV of atherosclerosis?
Death of foam cells leads to extracellular cholesterol deposition with a necrotic core.
Formation of a smooth muscle cell rich fibrous cap.
Macrophages with lipids can also die and release their cholesterol, formation of a necrotic core, they release cholesterol which may crystallize.
What is step V of atherosclerosis?
Upon aging the plaque cell death results in calcium depositions, that make arterial wall hard
Youg et loss of elasticity.
hardening of the vessel wall (sclerosis) result of dying macrophages that release their cholesterol
What is outward/inward remodelling?
INward: stenosis and reduced flow, no acute clinical symptoms
What is inward remodelling?
Stenosis in arteries of the leg
- intermittent claudication -> affects the function of th eleg
- gradual process, no acute clincal manifestation
What is the last step of atherosclerosis?
Atherosclerotic lesions step further.
Triggers of atherosclerosis continue to be present.
Inflammatory cells produce matrix degrading enzymes, those enzymes may affect the proective fibrous cap from the atheroscleoritc lesios.
thinning and rupture of the protective fibrous cap.
You get exposure of thrombenic materials to blood stream.
Obstruction of vessel lumen and flow (within hours)
Acute clinical manifestation
Thinning of the cap results in formation of a thrombus. Thrombus occludes the blood flow and artery loses it sf ucntion
What is mycoardial infarction?
Ischamiea of heart muscle tissue -> infarction -> loss of function
Impact on heart dpeending on location thrombus and rate endogenous fibrinolysis, when a thrombus is ofrmed and own fibronlysis is able to remove.
Than the impact is removesd, so imporant i determining the clincal outcome
What is cerebrovascular accident or ischaemic stroke?
Impact dependning on location and success/failure fibrinolysis, whether plasmin can be generated to remove the clot or not
Transiet ischaemic attack (thrombus is resolved)
ischemic stroke (aphasia paralyssi
What are side effects of therapeutic stimulation of fibrinolysis?
What are the most important effects of atheroma?
What are risk factors for atherosclerosis?
- advanced age
- male sex
- having close relatives who have some complication of atherosclerosis (eg coronary heart disease or stroke)
- genetic abnormalities, eg familial hypercholesterolemia
Modifiable:
- diabetes or impaired glucose tolerance (IGT)
- dyslipoproteinemia (unhealthy patterns of serum proteins carrying fats and cholesterol)
- tobacco smoking, increases risk by 200% after several pack years
- having high blood pressure, on its own increasing risk by 60%
What is the pathofysiology of atherosclerosis?
Lesion progression occurs through interactions of modified lipoproteins, monocyte-derived macrophages, T-lymphocytes, and the normal cellular constituent of the arterial wall.
The contemporary view of atherosclerosis is expressed by the response-to-injury hypothesis.
What is the response-to-injury hypothesis?
- accumulation of lipoproteins
- monocyte adhesion to the endotheliumm
- factor release and paltelet adhesion
- SMC prolifeartionds and EcM production
What is step 1 in developing atheroscloeris?
You get accumulation of foam histiocytes those are laden with lipids.
What is step 2 in developing atherosclerosis?
- lipids accumulate, free and in foamy histiocytes
- smooth muscle cells migrate from the media and proliferate
- fibrosis develops around the lipid and forms a cap over te helsisn
What is step 3 in developing atherosclerosis?
Ulcers and fissures of the fibrous cap reveal plaque contents resulting in thrombosis.
The plaque may undergo calcification, visible on X-ray
Inflmmation associated with the plaque destroys the media which undergoes fibrosis and is weakened
Which arteries are involved in atherosclerosis?
The branchial arteries are spared.
The renal arteries are spared (except in diabetes)
Maximum atheroma occurs at sites of haemodynamic stress: bifurcations, carotid bifurcation, aorta bifurcation
What vascular consequences has atheroma?
Lumenal occlusion: infarction
Embolism: ischaemia and infarction
Weakened wall: aneurysm
What is an symptom of lumenal narrowing?
What are risk factors for plaque rupture?
large necrotic center with many foam cells
inflammation
T lymphocytes (activation of macrophages and cytokines)
macrophages (production of metalloproteinases and cytokines)
increased blood pressure and stress
hemorrhage in plaque
What consequences of atherosclerosis in heart, brain, aorta, peripheral arteries?
Brain: infarction/stroke (vascular) dementia
Aorta: aneurysm with rupture
Peripheral arteries: ischemia of legs with claudicatio and gangrene, ischemia of organs
What are light microscopy of mycoardial infarction?
> 3 hr: loss of enzymes (LDH) and desmin
6-12 hr: early coagulation necrosis + some neutrophils
12-72 hr: heavy coagulation necrosis + many neutrophils
3-7 days: decrease of neutrophils and icnrease of marophages and lymphocytes
7-14 days: granulation tissue
2-8 weeks: formation of scar tissue
> 8 weeks: complete scar
What complications in myocardial infarction?
Pump failure (cardiogenic shock with > 40% volume of infarction)
Thrombosis (risk of emboli)
Aneurysm (risk of thrombosis, etc)
Ruptures:
- free wall: tamponade
- papillary muscle: valve insufficiency
- septum: shunting and heart failure
What complaints can be in the legs due to infarction?
the patient experiences pain in the calf on walking claudication.
This is relieved by rest and the patien'ts progress is punctuated by alternate walking and resting; intermittend claudication
Thrombosis may develop over an atheromatous plaque int he femoral (or other supplying) artery resulting in infarction of al tissues served (gangrene)
This can also occur in severe stenotic atheroma if seomthing else reduces blood flow, eg dvelopment of cardiac failure
What are treatment and drugs for atheroma?
- healthy diet and exercising, stop smoking
Cholesterol medications (statins)
- lowering low-density lipoprotein (LDL), cholesterol, can slow, stop or even reverse the buildup of fatty deposits in arteries
Anti-platelet medications (aspirin) to prevent clotting platelets in narrowed arteries, form a blood clot and cause further blockage.
Anticoagulants (heparin) can help thin blood to prevent clots from forming
Blood pressure medications (beta blockers angiotensin converting enzyme (ACE) inhibitors can help slow the progression of atherosclerosis
What surgical treatments in atheroma?
bypass surgery
angioplasty
endarterectomy
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